Yang Jae-Wook, Jung Won-Kyo, Lee Chang-Min, Yea Sung Su, Choi Yung Hyun, Kim Gi-Young, Lee Dae-Sung, Na Giyoun, Park Sae-Gwang, Seo Su-Kil, Choi Jung Sik, Lee Young-Min, Park Won Sun, Choi Il-Whan
Department of Ophthalmology, Busan Paik Hospital, College of Medicine Inje University , Busan , Republic of Korea .
Immunopharmacol Immunotoxicol. 2014 Oct;36(5):371-7. doi: 10.3109/08923973.2014.953957. Epub 2014 Aug 25.
Expression of various inflammatory mediators in corneal fibroblasts contributes to corneal inflammation.
The purpose of this study was to assess the possible effects of caffeic acid phenethyl ester (CAPE) on the expression of inflammatory mediators during an inflammatory response in human corneal fibroblasts.
The levels of interleukin (IL)-6, monocyte chemotactic protein (MCP)-1, and intercellular adhesion molecule-1 (ICAM-1) from IL-1β-exposed human corneal fibroblasts were measured with enzyme-linked immunosorbent assays (ELISA). The regulatory mechanisms of CAPE on cellular signaling pathways were examined using Western blot and electrophoretic mobility shift assays. A functional validation was carried out by evaluating the inhibitory effects of CAPE on neutrophil and monocyte migration in vitro.
CAPE inhibited the expression of IL-6, MCP-1 and ICAM-1 induced by the pro-inflammatory cytokine IL-1β in corneal fibroblasts. The activation of AKT and NF-κB by IL-1β was markedly inhibited by CAPE, whereas the activity of mitogen-activated protein kinases (MAPKs) was not affected. CAPE significantly suppressed the IL-1β-induced migration of differentiated (d)HL-60 and THP-1 cells.
These anti-inflammatory effects of CAPE may be expected to inhibit the infiltration of leukocytes into the corneal stroma in vivo.
角膜成纤维细胞中多种炎症介质的表达会导致角膜炎症。
本研究旨在评估咖啡酸苯乙酯（CAPE）在人角膜成纤维细胞炎症反应过程中对炎症介质表达的可能影响。
采用酶联免疫吸附测定（ELISA）法检测白细胞介素（IL）-6、单核细胞趋化蛋白（MCP）-1和细胞间黏附分子-1（ICAM-1）在暴露于IL-1β的人角膜成纤维细胞中的水平。使用蛋白质印迹法和电泳迁移率变动分析法检测CAPE对细胞信号通路的调节机制。通过评估CAPE对体外中性粒细胞和单核细胞迁移的抑制作用进行功能验证。
CAPE抑制了促炎细胞因子IL-1β诱导的角膜成纤维细胞中IL-6、MCP-1和ICAM-1的表达。CAPE显著抑制了IL-1β对AKT和NF-κB的激活，而丝裂原活化蛋白激酶（MAPK）的活性未受影响。CAPE显著抑制了IL-1β诱导的分化型（d）HL-60和THP-1细胞的迁移。
CAPE的这些抗炎作用有望在体内抑制白细胞向角膜基质的浸润。
